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Pharm Year 3 Sem1 patient > gluacoma > Flashcards

gluacoma Flashcards

1
Q

what is glaucoma?

A

blanket term for a variety of conditions

• Common factor is acquired progressive neuropathy (if untreated)
• Optic nerve damage
• Visual field loss
Eventual blindness

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2
Q

what are the risk factors of glaucoma?

A 
• Normally asymptomatic
• High IOP (>21mmHg)
• Family history of glaucoma
• Race - afro Caribbean 
• Systemic hypertension
• Cardiovascular disease
• Migraine
Previous ocular disease
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3
Q

what are the main aims of a glaucoma treatment?

A
  • Reduce IOP
    • <16-20mmHg depending on patient
  • Drug to have sufficient duration of action (esp eyedrops)
    • Patient compliance
  • Provides:
    • Preservation of visual field
    • No loss of effect over time
    • Compatibility with other treatments
    • No topical or systemic side effects
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4
Q

what drugs are used to treat glaucoma?

A

prostaglandins and prostamide analogues

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5
Q

what types of gluacoma are there?

A

primary and secondary
open angle

close angle

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6
Q

what are the symptoms of glaucoma

A

asymptomatic

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7
Q

describe the aetiology of glaucoma

A

impaired drainage of aqueous humour

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8
Q

how is closed angle glaucoma treated

A

surgery

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9
Q

how is aqueous humour produced?

A 
large blood supply
fluid from capillaries
into epithelial cells makes humour
comes round the lens
comes out of the pupil
into the side
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10
Q

describe the main parts of the eye?

A

iris, pupil, lens, colliery muscle

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11
Q

where is aqueous humour produced?

A

outermost cells - epithelial cells of the eye

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12
Q

open angle

A

angle between the iris and the sclera

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13
Q

trabecular meshwork

A

aq humour flows through space cells into the collector channel and out the episcleral vein
because pressure in episceral vein is lower
8mmHg to 16mmHg

80% fluid through

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14
Q

uveoscleral outflow

A

20% flow

bypass trabecular meshwork
sclera ancillary body
more resistance as there is much less space for fluid to move
goes through much slower

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15
Q

Prostaglandins

A

PGE required for production of aq humour but not stable
PG f2alpha more stable

latanoprost, tafluprost and travoprost
(esters)

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16
Q

prostamides analogues?

A

bimatoprost

prostamide f2alpha precursor

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17
Q

why use prostaglandins analogues?

A

produced naturally in most cells
involved in aq humour outflow

1st choice clinically: uniquely decrease IOP , most effective

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18
Q

how do prostaglandin analogues work ?

A

act on the PG2Falpha receptor
ester converted back to acid (by esterase’s in the eye)
GPCR (g alpha q)

activates PLC, DAG, IP3

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19
Q

which glaucoma drugs act by increasing aqueous outflow?

A

prostaglandin analogues - increase uveoscleral outflow
praostamide analogues - inc trabecular outflow
parasympamimetic drugs - inc trabecular outflow

20
Q

which glaucoma drugs act by decreasing aqueous humour production ?

A

beta blockers -

alpha selective -

21
Q

name the parasympathomimetic drugs?

A

pilocarpine

22
Q

where are Fp receptors found?

A

• Ciliary body & muscle, sclera (mainly)
• Iris sphincter (small amounts)
Trabecular meshwork cells (few present)

23
Q

advantages of prostaglandin analogues and prostamide analogues

A

once a day (night)
good tolerability
Efficacious
reduce IOP by 35%

24
Q

describe the main action of prostamide analogues

A

increases both trabecular outflow and uveoscleral outflow via binding to F2a receptors and prostamide receptors

25
Q

describe the main action of prostaglandin analogues

A

reduced resistance to uveoscleral outflow by remodelling extracellular matrix :
inc matrix metalloproteinases
decreases collagen and extracellular matrix
decreases resistance of colliery muscle and sclera to increase outflow
most likely via FP receptors -

26
Q

side effects of prostaglandin analogues

A

red eye
inc pigmentation of iris, eyelash and periocular skin,
eyelash growth
precipitate or worsen cystoid macular oedema in aphasic eyes
sensitivity to light
contraindicated in pregnancy - can induce labour and affect cell division

27
Q

how are beta blockers used to treat glaucoma ?

A

decrease aqueous humour production by block beta receptors , inhibiting cAMP production

NA+K+2Cl- co-transoporter activation and Cl- efflux don’t occur

decreased ion transport decreases aq humour production as osmotic gradient not present

28
Q

advantages of beta blockers

A

rapid onset
well tolerated
20-30 % reduction
compatible with other drugs

29
Q

Disadvantages of beta blockers

A

more easily absorbed systemically
systemic side effects
efficacy declines over time
twice daily admin or once daily with certain preparations

30
Q

side effects of beta blockers

A

generally systemic
cardiovascular - bradycardia,hypotension,peripheral,vasoconstriction,impotence,
C/I in heart block,failure

bronchial : constriction of bronchioles : c/I in asthma and COPD

diabetes: block sympathetic response - mask hypo

31
Q

advantages of fixed dose combination

A 
different classes of drugs - additive effects
patient compliance
reduced exposure to preservatives
avoid washout effect of 2nd drop
decrease treatment dose
decrease patient cost - 1 Rx charge
32
Q

describe treatment pathway for glaucoma

A

Prostaglandin/prostamide analogues analogues
beta blockers
fixed combination
carbonic anhydrase inhibitor

33
Q

how do carbonic anhydrases inhibitors work?

A

inhibit carbonic anhydrases in cilliery epithilium - reduced ion gradient - reduced aq humour production

34
Q

name a systemic CAI

how and when are systemic CAIs used?

A

drug: acetozolamide
not absorbed topically, not v lipophilic

when IOP is very elevated/ emergency
injected
used in OAG,secondary glaucoma, per iteratively in acute angle closure glaucoma

35
Q

acetazolamide side effects

A

sulfanimde derivative - allergies and blood disorders
enzymes across the body :
GI effects, diuresis, drowsiness, acid/base imbalance depression parasthesias

36
Q

how can acetazolamide be adapted for ocular use?
How does this change the drug?
give examples

A

modify to giver better lips solubility
decreasing side effects
more selective for CA-II enzyme
Dorzolamide and brinzolamide

37
Q

describe the effects of topical CAIs. When are they used

A

20% IOP reduction
adjunct therapy or single therapy if beta blockers not indicated
local side effects

38
Q

describe side effects of topical CAIs

A

transient burning, stinging
pH brinzolamide drops (7.5,5.6-6.0)

blurred vision conjunctival hyperaemia
transient myopia, blepharitis, allergic conjunctivitis

taste disturbances, dry mouth, headache

39
Q

describe mechanism of action for alpha2 adrenoreceptor agonists

A

alpha receptor selective
receptors are on the ciliary, conjunctival and corneal epithelial cells

decrease aq secretion by decreasing cAMP - decrease ion transport- decrease aq secretion
decreases ultrafiltration
inc uveosceral outflow

40
Q

advantages of a2 adrenoreceptor agonists

A

no mydriasis
no vasoconstriction
little effect on CV system

41
Q

why can a2 adrenorecptor agonists be considered neuroprotective?

A

preserve optic nerve and retinal ganglion cells

42
Q

give an example of a2 adrenorecptor drugs

briefly describe their characteristics

A

brimonidine - selective
rapid 2hr onset
apraclonidine - less selective, short term use (causes tachy) used post laser eye surgery to prevent IOP rise

43
Q

a2 adrenorecptor agonist side effets

A

local - allergy, sting, burn ,blurred vision, photophobia

systemic - hypotension

44
Q

mechanism of parasympathomimetic drugs?

A 
m3 receptor agonists 
contract ciliary muscle 
pull scleral spur 
opens trabecular meshwork 
inc trabecular outflow 
decrease IOP

last 6hr
cyclical effect on IOP through day
QDS patient compliance reduced

45
Q

parathesiais

A

burning tingling of skin - experienced with carbonic anhydrases

Pharm Year 3 Sem1 patient (12 decks)

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